Evidence map›Paper›PMID 37595508›Full record

ArticleSeminars in arthritis and rheumatism2023

Gene-respiratory disease interactions for rheumatoid arthritis risk.

Vanessa L Kronzer, Keigo Hayashi, Cynthia S Crowson, John M Davis, Gregory C McDermott, Jing Cui, Elena Losina, Pierre-Antoine Juge, James R Cerhan, Jeffrey A Sparks

Open access · greenAbstract read
In one paragraph

Article in Seminars in arthritis and rheumatism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Vanessa L KronzerDivision of Rheumatology, Mayo Clinic, Rochester, MN, USA. Electronic address: kronzer.vanessa@mayo.edu.
Keigo HayashiDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital; Harvard Medical School, Boston, USA. Electronic address: khayashi3@bwh.harvard.edu.
Cynthia S CrowsonDivision of Rheumatology, Mayo Clinic, Rochester, MN, USA; Department of Quantitative Health Sciences, Mayo Clinic, Rochester, Minnesota, USA. Electronic address: crowson@mayo.edu.
John M DavisDivision of Rheumatology, Mayo Clinic, Rochester, MN, USA. Electronic address: Davis.John4@mayo.edu.
Gregory C McDermottDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital; Harvard Medical School, Boston, USA. Electronic address: GMCDERMOTT@PARTNERS.ORG.
Jing CuiDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA. Electronic address: JCUI@BWH.HARVARD.EDU.
Elena LosinaDepartment of Orthopedic Surgery, Brigham and Women's Hospital, Boston, USA. Electronic address: elosina@bwh.harvard.edu.
Pierre-Antoine JugeDept of Rheumatology, DMU Locomotion, INSERM UMR1152, Hôpital Bichat-Claude Bernard, APHP, Université de Paris, Paris, France. Electronic address: pjuge@bwh.harvard.edu.
James R CerhanDepartment of Quantitative Health Sciences, Mayo Clinic, Rochester, Minnesota, USA. Electronic address: Cerhan.James@mayo.edu.
Jeffrey A SparksDivision of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital; Harvard Medical School, Boston, USA. Electronic address: JSPARKS@BWH.HARVARD.EDU.
Brigham and Women's Hospital · USMayo Clinic in Arizona · USMayo Clinic in Florida · USUniversité Claude Bernard Lyon 1 · FR

Funding

HEART DISEASE IN RHEUMATOID ARTHRITISR01AR046849 · NIAMS · MAYO CLINIC ROCHESTER · PI CROWSON, CYNTHIA S · 2000 to 2022
$11.3M
MECHANISMS OF ARTHRITIC &DERMATOLOGY DISORDERST32AR007530 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Michael B. Brenner, Ellen M Gravallese · 1986 to 2026
$10.4M
VERITY: Value and Evidence in Rheumatology using bioInformaTics, and advanced analYticsP30AR072577 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Daniel Hal Solomon · 2017 to 2026
$9.8M
Joint Biology Consortium Resource-based CenterP30AR070253 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Peter A Nigrovic, Jeffrey Andrew Sparks · 2016 to 2026
$9.4M
Rheumatoid Arthritis-Related Autoantibodies, Articular Inflammation, and RA-Associated Interstitial Lung DiseaseR01AR077607 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SPARKS, JEFFREY ANDREW · 2021 to 2025
$3.7M
Immunologic and Clinical Sequelae after COVID-19 in Patients with Systemic Autoimmune Rheumatic DiseasesR01AR080659 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Jeffrey Andrew Sparks · 2023 to 2026
$2.9M
NIAMS NIH HHS P30 AR070253NIAMS NIH HHS P30 AR072577NIAMS NIH HHS R01 AR046849NIAMS NIH HHS R01 AR077607NIAMS NIH HHS R01 AR080659NIAMS NIH HHS T32 AR007530
6 · The paper itself

Abstract

objectiveWe aimed to identify gene by respiratory tract disease interactions that increase RA risk.

methodsIn this case-control study using the Mass General Brigham Biobank, we matched incident RA cases, confirmed by ACR/EULAR criteria, to four controls on age, sex, and electronic health record history. Genetic exposures included a validated overall genetic risk score (GRS) for RA, a Human Leukocyte Antigen (HLA) GRS for RA, and the MUC5B promoter variant, an established risk factor for RA-associated interstitial lung disease (ILD). Preceding respiratory tract diseases came from diagnosis codes (positive predictive value 86%). We estimated attributable proportions (AP) and multiplicative odds ratios (OR) with 95% confidence intervals (CI) for RA for each genetic and respiratory exposure using conditional logistic regression models, adjusting for potential confounders.

resultsWe identified 653 incident RA cases and 2,607 matched controls (mean 54 years, 76% female). The highest tertile of the overall GRS and the HLA GRS were both associated with increased RA risk (OR 2.28, 95% CI 1.89,2.74; OR 2.02, 95% CI 1.67-2.45). ILD and the HLA GRS exhibited a synergistic relationship for RA risk (OR for both exposures 4.30, 95% CI 1.28,14.38; AP 0.51, 95% CI-0.16,1.18). Asthma and the MUC5B promoter variant also exhibited a synergistic interaction for seropositive RA (OR for both exposures 2.58, 95% CI 1.10,6.07; AP 0.62, 95% CI 0.24,1.00).

conclusionILD-HLA GRS and asthma-MUC5B promoter variant showed synergistic interactions for RA risk. Such interactions may prove useful for RA prevention and screening.

Indexed as

Arthritis, RheumatoidAsthmaLung Diseases, InterstitialCase-Control StudiesFemaleHumansMaleRisk FactorsEpidemiologyGenetics, MUC5BInteractionRespiratory diseaseRespiratory tract diseasesRheumatoid arthritis

Identifiers

PMID37595508
PMCPMC10840753
OpenAlexW4385781944

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.